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Göteborgs universitets publikationer

Effects of ghrelin on anorexia in tumor-bearing mice with eicosanoid-related cachexia

Författare och institution:
Wenhua Wang (Institutionen för kliniska vetenskaper, sektionen för kirurgi och kirurgisk gastroforskning); Marianne Andersson (Institutionen för kliniska vetenskaper, sektionen för kirurgi och kirurgisk gastroforskning); Britt-Marie Iresjö (Institutionen för kliniska vetenskaper, sektionen för kirurgi och kirurgisk gastroforskning); Christina Lönnroth (Institutionen för kliniska vetenskaper, sektionen för kirurgi och kirurgisk gastroforskning); Kent Lundholm (Institutionen för kliniska vetenskaper, sektionen för kirurgi och kirurgisk gastroforskning)
Publicerad i:
International journal of oncology, 28 ( 6 ) s. 1393-400
1019-6439 (Print)
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
Ghrelin is a novel brain-gut peptide that stimulates food intake and may secondarily increase body weight via a growth hormone secretagogue receptor (GHS-R). Tumor-bearing mice (MCG101), characterized by anorexia, fat loss and muscle wasting due to increased concentration of PGE2 and proinflammatory cytokines (IL-1beta, IL-6, TNF-alpha), were provided ghrelin i.p. at a low (20 microg/day) and high dose (40 microg/day) to examine the ability of ghrelin to counteract tumor-induced anorexia. Immunohistochemical staining and Western blot analyses were used to identify GHS-R expression in the brain as well as its relationship to NPY expression in hypothalamic neurons. GHS-R mRNA in hypothalamus and ghrelin mRNA in gastric fundus were quantified by RT-PCR. Body composition was determined by carcass extractions. GHS-R expression in hypothalamus and plasma ghrelin levels were significantly increased in freely-fed tumor-bearing mice, while gastric fundus expression of ghrelin was unaltered compared to non-tumor-bearing mice (controls). Ghrelin treatment increased food intake, body weight and whole body fat at both low and high doses of ghrelin in normal controls, while tumor-bearing mice showed improved intake and body composition at the high dose of ghrelin only. Exogenous ghrelin normalized the GHS-R expression in hypothalamus from tumor-bearing mice without alterations in the gastric fundus expression of ghrelin. Tumor growth was not altered by exogenous ghrelin. Our results indicate that MCG 101-bearing mice became ghrelin resistant despite upregulation of hypothalamic GHS-R expression, which confirms similar indirect observations in cancer patients. Thus, other factors downstream of the ghrelin-GHS-R system appear to be more important than ghrelin to explain cancer-induced anorexia.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Animals, Anorexia/*drug therapy/etiology, Cachexia/*drug therapy/etiology, Eicosanoids/*adverse effects, Energy Intake, Female, Growth Hormone/therapeutic use, Mice, Mice, Inbred C57BL, Peptide Hormones/*therapeutic use, RNA, Messenger/genetics, Receptors, G-Protein-Coupled/genetics, Reverse Transcriptase Polymerase Chain Reaction, Sarcoma, Experimental/complications/*pathology
Postens nummer:
Posten skapad:
2007-09-21 13:07

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